The discovery of AP2's role may lead to better control of type 2 diabetes and other metabolic diseases, the researchers say. They tested changing the levels of the hormone on lean and normal mice.

"Recombinant aP2 stimulates glucose production and gluconeogenic activity in primary hepatocytes in vitro and in lean mice in vivo. In contrast, neutralization of secreted aP2 reduces glucose production and corrects the diabetic phenotype of obese mice," the paper stated.

"We suspect this communication system between adipose tissue and liver may have evolved to help fat cells command the liver to supply the body with glucose in times of nutrient deprivation," said senior author Gökhan S. Hotamisligil in a Harvard press release. "However, when the engorged fat cells lose control over this signal in obesity, the blood levels of aP2 rise, glucose is poured into the bloodstream and cannot be cleared by other tissues. The result is high blood glucose levels and type 2 diabetes."

Hotamisligil chairs the Department of Genetics and Complex Diseases at HSPH.

The study research was funded in part by the National Institutes of Health, the American Diabetes Association; and fellowships from the Manpei Suzuki Diabetes Foundation and the Japan Society for the Promotion of Science.

While insulin is the main hormone involved in diabetes types 1 and 2, a number of other important hormones have been discovered since. These include amylin, secreted by the same beta cells of the pancreas that secrete insulin. The discovery of amylin gave its name to Amylin Pharmaceuticals, the San Diego-based biotech company purchased in 2012 by Bristol-Myers Squibb.

And another biotech company has licensed the technology used in the study, UCB, or Union Chimique Belge, based in Belgium with U.S. offices.